Signaling Pathways in Endometrial Cancer Cells
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".
Deadline for manuscript submissions: 20 January 2026 | Viewed by 7886
Special Issue Editor
Special Issue Information
Dear Colleagues,
Endometrial cancer (EC) develops from the uterine endometrial epithelium. Recent reports indicate that oncogenic mutations are already present in normal endometrium, suggesting that altered signaling pathways are involved in carcinogenesis. The PI3K/AKT/mTOR pathway is the most frequent activated signaling pathway in EC cells. This pathway governs cell proliferation, metabolism, and DNA damage repair. The RAS/MAPK pathway is also important for EC cell growth. However, inhibitors for both signaling pathways have not been successful in clinical trials. Historically, EC has been classified into two types according to hormone dependence. ER, PgR-positive, hormone-dependent ECs are sensitive to progesterone and aromatase inhibitors that partially block both the PI3K/AKT/mTOR and RAS/MAPK pathways. Recently, four molecular classifications have been proposed according to the TCGA project. POLE ultramutated and MSI subtypes are susceptible to immune checkpoint inhibitors. In contrast, the other two subtypes are resistant to immunotherapy. Interestingly, CDK4/6 and Wee1 inhibitors are effective for CN-L and CN-H subtypes, respectively. These findings indicate that modification of various signaling pathways may be useful in the treatment of EC.
Under this perspective, this Special Issue aims to describe the current advances in basic and translational research that focus on “Signaling Pathways in Endometrial Cancer Cells”.
Dr. Tomohiko Fukuda
Guest Editor
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Keywords
- endometrial cancer
- cellular signaling
- cell metabolism
- DNA damage repair pathway
- the PI3K/AKT/mTOR pathway
- the RAS/MAPK pathway
- molecular classification
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